PURPOSE: To evaluate EGFR and HER2 copy number changes and to assess their significance to tumor progression in a large group of patients with larynx cancer through the construction of a tissue microarray (TMA) consisting of 1,385 biopsies. METHODS: Fluorescent in situ hybridization (FISH) was applied to analyze the tumors. FISH was successful for EGFR in 1,080 (77.98%) and for HER2 in 683 (49.31%). RESULTS: HER2 was amplified in 1.02% of cases. Amplification did not correlate with the tumor phenotype-clinical stage, and grade. The low frequency of amplification of HER2 oncogene in larynx tumors showed that the mechanism responsible for the high level of receptor overexpression still remains unclear in the majority of cases. Amplification of EGFR was found in 10.37% of cases. The analysis revealed a lack of correlation between amplification of the oncogenes and the tumor phenotype. We observed a lack of difference between the samples of primary tumors and advanced disease carcinomas--tumors with regional/distant metastases and recurrent tumors regarding oncogene amplification. CONCLUSION: These results suggest that EGFR amplification is a relatively rare event in larynx carcinogenesis that obviously does not predispose to tumor progression.
PURPOSE: To evaluate EGFR and HER2 copy number changes and to assess their significance to tumor progression in a large group of patients with larynx cancer through the construction of a tissue microarray (TMA) consisting of 1,385 biopsies. METHODS: Fluorescent in situ hybridization (FISH) was applied to analyze the tumors. FISH was successful for EGFR in 1,080 (77.98%) and for HER2 in 683 (49.31%). RESULTS:HER2 was amplified in 1.02% of cases. Amplification did not correlate with the tumor phenotype-clinical stage, and grade. The low frequency of amplification of HER2 oncogene in larynx tumors showed that the mechanism responsible for the high level of receptor overexpression still remains unclear in the majority of cases. Amplification of EGFR was found in 10.37% of cases. The analysis revealed a lack of correlation between amplification of the oncogenes and the tumor phenotype. We observed a lack of difference between the samples of primary tumors and advanced disease carcinomas--tumors with regional/distant metastases and recurrent tumors regarding oncogene amplification. CONCLUSION: These results suggest that EGFR amplification is a relatively rare event in larynx carcinogenesis that obviously does not predispose to tumor progression.
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